Non‐alcoholic hepatic steatosis and its relation to increased plasma biomarkers of inflammation and endothelial dysfunction in non‐diabetic men. Role of visceral adipose tissue

Targher, Giovanni; Bertolini, Lorenzo; Scala, Luca; Zoppini, Giacomo; Zenari, Luciano; Falezza, Giancarlo

doi:10.1111/j.1464-5491.2005.01646.x

Cited by 160 publications

(141 citation statements)

References 25 publications

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“…[7][8][9][10] These findings might have important clinical and public health implications. Since NAFLD patients are at increased cardiovascular risk, the casual detection of NAFLD on an ultrasound examination should alert to the possible coexistence of multiple underlying cardiovascular risk factors warranting evaluation and treatment as much as the risk for advancing liver disease.…”

Section: Associations Between Liver Histology and Early Carotid Athermentioning

confidence: 92%

Associations Between Liver Histology and Early Carotid Atherosclerosis in Subjects With Nonalcoholic Fatty Liver Disease *

Targher

2005

Hepatology

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Section: Associations Between Liver Histology and Early Carotid Athermentioning

confidence: 92%

Associations Between Liver Histology and Early Carotid Atherosclerosis in Subjects With Nonalcoholic Fatty Liver Disease *

Targher

2005

Hepatology

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“…1 In most industrialized countries, the prevalence of NAFLD continues to rise along with obesity, 2 because it is developed as the result of conditions associated with obesity, including hepatic fat accumulation, oxidative stress, insulin resistance and adiposity. 3,4 NAFLD is frequently conceptualized as a four-step process, including simple steatosis, steatohepatitis accompanied with inflammation and fibrosis, cirrhosis and hepatocellular carcinoma. Thus, the most effective precaution against NAFLD might be to interrupt initial steps, simple steatosis, and its inflammatory form, steatohepatitis.…”

Section: Introductionmentioning

confidence: 99%

“…1 The principle characteristic of hepatic steatosis is the excessive accumulation of triglycerides (TGs), which are available from lipids newly synthesized in the liver or a surplus supply of free fatty acid (FFA) released from adipose tissue. Steatohepatitis is aggravated by adipose tissue inflammation 4 and the imbalance of adipocytokines (that is, leptin, adiponectin and tumor necrosis factor (TNF) a). 5 Recently, a transcription factor carbohydrate responsive element binding protein (ChREBP) has emerged as a central determinant of hepatic lipogenesis through its transcriptional control of stearoyl CoA desaturase-1, acetyl CoA carboxylase and fatty acid synthase, 6 and hepatic insulin resistance by the inhibition of thymoma viral protooncogene (Akt).…”

Section: Introductionmentioning

confidence: 99%

Daidzein supplementation prevents non-alcoholic fatty liver disease through alternation of hepatic gene expression profiles and adipocyte metabolism

et al. 2010

Int J Obes

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Introduction: Globally, non-alcoholic fatty liver disease (NAFLD) continues to rise and isoflavones exert antisteatotic effects by the regulation of hepatic lipogenesis/insulin resistance or adiposity/a variety of adipocytokines are related to hepatic steatosis. However, there is very little information regarding the potential effects of daidzein, the secondary abundant isoflavone, on NAFLD. Here, we have assessed the hepatic global transcription profiles, adipocytokines and adiposity in mice with high fat-induced NAFLD and their alteration by daidzein supplementation. Methods: C57BL/6J mice were fed with normal fat (16% fat of total energy), high fat (HF; 36% fat of total energy) and HF supplemented with daidzein (0.1, 0.5, 1 and 2 g per kg diet) for 12 weeks. Results: Daidzein supplementation (X0.5 g per kg diet) reduced hepatic lipid concentrations and alleviated hepatic steatosis. The hepatic microarray showed that daidzein supplementation (1 g per kg diet) downregulated carbohydrate responsive element binding protein, a determinant of de novo lipogenesis, its upstream gene liver X receptor b and its target genes encoding for lipogenic enzymes, thereby preventing hepatic steatosis and insulin resistance. These results were confirmed by lower insulin and blood glucose levels as well as homeostasis model assessment insulin resistance scores. In addition, daidzein supplementation inhibited adiposity by the upregulation of genes involved in fatty acid b-oxidation and the antiadipogeneis, and moreover augmented antisteatohepatitic leptin and adiponectin mRNA levels, whereas it reduced the mRNA or concentration of steatotic tumor necrosis factor a and ghrelin. Conclusions: These findings show that daidzein might alleviate NAFLD through the direct regulation of hepatic de novo lipogenesis and insulin signaling, and the indirect control of adiposity and adipocytokines by the alteration of adipocyte metabolism.

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“…10,11 Hepatic steatosis has also been associated with elevated serum levels of markers of inflammation and endothelial dysfunction. 12 These factors suggest a biologically plausible mechanism of increased risk of CAD in at least a subset of HCV-infected persons.…”

mentioning

confidence: 97%

Higher Prevalence and More Severe Coronary Artery Disease in Hepatitis C Virus-infected Patients: A Case Control Study

Satapathy

Kim

Kataria

et al. 2013

Journal of Clinical and Experimental Hepatology

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Background: An association of Coronary artery disease (CAD) with hepatitis C (HCV) has been suggested, but definitive data are still lacking. Aim: Our study sought to estimate the prevalence and severity of CAD in HCV patients compared to with age-, sex-, and race-matched controls without HCV infection. Subjects and methods: 63 HCV-infected patients were compared with 63 age, race, and sex-matched controls without HCV infection undergoing coronary angiography for evaluation of CAD. CAD was defined as more than a 50% blockage in any of the proximal coronary arteries on angiogram. The severity of the stenosis was defined by the modified Reardon severity scoring system: <50% stenosis of the luminal diameter, 1 point; 50-74%, 2 points; 75-99%, 3 points; 100% or total obstruction, 4 points. The points for each lesion in the proximal coronary circulation were summed to give the score for severity. Results: A significantly higher prevalence of CAD was noted in the HCV population (69.8% vs. 47.6%, = 0.01). The combined Reardon's severity score in the HCV group was significantly higher compared to the controls (6.26 ± 5.39 vs. 2.6 ± 3.03, P < 0.0005). Additionally, significant multivessel CAD (>50% stenosis and $2 vessels involved) was also noted significantly more commonly in the HCV group compared to controls (57.1% vs. 15.9%, P < 0.0005). Conclusion: In this retrospective study the prevalence and severity of CAD was higher in HCV patients who were evaluated for CAD by angiogram compared with matched non-HCV patients. HCV-positive status is potentially a risk factor for CAD. ( J CLIN EXP HEPATOL 2013;3: 186-191)

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Non‐alcoholic hepatic steatosis and its relation to increased plasma biomarkers of inflammation and endothelial dysfunction in non‐diabetic men. Role of visceral adipose tissue

Abstract: These results indicate that, in non-smoking, non-diabetic men, the significant increase of plasma biomarkers of inflammation and endothelial dysfunction in the presence of non-alcoholic HS is largely mediated by abdominal visceral fat accumulation.

Cited by 160 publications

References 25 publications

Associations Between Liver Histology and Early Carotid Atherosclerosis in Subjects With Nonalcoholic Fatty Liver Disease *

Associations Between Liver Histology and Early Carotid Atherosclerosis in Subjects With Nonalcoholic Fatty Liver Disease *

Daidzein supplementation prevents non-alcoholic fatty liver disease through alternation of hepatic gene expression profiles and adipocyte metabolism

Higher Prevalence and More Severe Coronary Artery Disease in Hepatitis C Virus-infected Patients: A Case Control Study

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